KAPLAN - Physiology

Question 1

Arterial blood gases (ABGs) are used in:

Answer 1

acid - base disturbances: source for the diagnostic data for determining an acedemia or alkalemia (indicative of underlying acidosis or alkalosis).

Question 2

Three question method for acid base disturbances.

Answer 2

1. What is the osis? (if pH <7.35, then acidosis, if pH is >7.45, then alkalosis)
2. What is cause of osis?
3. Was there compensation?

Question 3

normal value of pH

Answer 3

normal pH = 7.4

normal range of pH 7.35 - 7.45

Question 4

For respiratory disturbances, what happens?

Answer 4

Kidneys alter total bicarbonate

Question 5

For respiratory compensation, what is compared?

Answer 5

Patient’s measure PCO2 verse a calculated (predicted) value.

Question 6

What is altered in the 4 primary disturbances?

Answer 6

altered concentration of H+

Acidosis (excess H+), alkalosis (deficiency of H+)

Question 7

What are the 4 primary disturbances?

Answer 7

1. respiratory acidosis: too much CO2
2. metabolic acidosis: addition of H+ (not of CO2 origin and/or loss of bicarbonate from the body
3. respiratory alkalosis: not enough CO2
4. metabolic alkalosis: loss H+ (not of CO2 origin) and/or addition of base to body

Question 8

normal systemic value for pH, HCO3-, PCO2?

Answer 8

pH = 7.4
HCO3- = -24 mEq/L
PCO2 = 40 mm Hg

Question 9

Acute changes in pH/HCO3- in the 4 primary disturbances?

Answer 9

1. respiratory acidosis: pH: DOWN, HCO3-: UP
2. metabolic acidosis: pH: UP, HCO3-: DOWNDOWN
3. respiratory alkalosis: pH: UP, HCO3-: DOWN
4. metabolic alkalosis: pH: UP, HCO3-: DOWNDOWN

Question 10

What is the CO2/HCO3- ratio in Respiratory acidosis for an acute (uncompensated) respiratory acidosis?

Answer 10

1 : 0.1 ratio of CO2 increase to HCO3- increase

Increasing CO2 drives the reaction to the right, thereby increasing HCO3-

Question 11

It causes a marked decrease in HCO3- because the addition of H+ consumes bicarbonate (drives reaction to the left).

Alternatively, an acidosis can be caused by loss of base (bicarbonate) to the body.

Answer 11

Metabolic acidosis

Question 12

What is the CO2/HCO3- ratio in Respiratory alkalosis for an acute (uncompensated) respiratory alkalosis?

Answer 12

1 : 0.2 ratio of CO2 decrease to HCO3- decrease

Decreasing CO2 drives the reaction to the left, thereby reducing HCO3-

Question 13

It causes a rise in HCO3- because the loss of H+ drives the reaction to the right.

Alternatively, an alkalosis can be caused by addition of base (bicarbonate) to the body.

Answer 13

Metabolic Alkalosis

Question 14

How do Kidneys compensate in respiratory acidosis?

Answer 14

The kidneys compensate by increasing HCO3- and eliminating H+ but the kidney take days to fully compensate.

1 : 0/35 ratio of CO2 increase to HCO3- increase in a chronic (compensated) respiratory acidosis.

Question 15

How is metabolic acidosis characterized and compensated?

Answer 15

Low pH and HCO3-. The drop in pH stimulates ventilation via peripheral chemoreceptors thus the respiratory system provides the first, rapid compensatory response.

Question 16

What is Winter’s equation and what is it used for?

Answer 16

Determines if the respiratory response is adequate.

Predicted PaCO2 = (1.5 x HCO3-) + 8

If predicted PaCO2 is 2 (±) then respiratory compensation has occurred.

Question 17

How do Kidneys compensate in respiratory alkalosis?

Answer 17

The kidneys compensate by Decreasing HCO3- and conserving H+ but the kidney take days to fully compensate.

1 : 0.5 ratio of CO2 decrease to HCO3- decrease in chronic (compensated) respiratory alkalosis

Question 18

maximum low for HCO3-

Answer 18

15 mEq/L

Question 19

in order to retain CO2, what is done and what equation is used?

Answer 19

ventilation decreases to retain CO2

It computes the PaCO2, which denotes appropriate compensation.

Expected PaCO2 = (0.7 x rise in HCO3-) + 40

If predicted PaCO2 is 2 (±) but should not exceed 55 mm Hg. the 40 represents the normal PaCO2

Question 20

When there is overcompensation, what caused it?

Answer 20

The body never overcompensates. There is likely a second disorder part from primary disorder.

Question 21

What does it mean when CO2 and HCO3- go in opposite direction?

Answer 21

There is a combined disturbance – either a combined (mixed) respiratory and metabolic acidosis or a combined (mixed) respiratory and metabolic alkalosis.

Question 22

Too much CO2

Answer 22

Respiratory acidosis

Question 23

Too little CO2

Answer 23

Respiratory alkalosis

Question 24

Normal value for NA+

Answer 24

140 mEq/L

Question 25

normal value for Cl-

Answer 25

104 mEq/L

Question 26

normal value HCO3-

Answer 26

24 mEq/L

Question 27

how to calculate Plasma Anion Gap (PAG) and its normal value?

Answer 27

PAG: NA+ - (Cl- + HCO3-) PAG: 12 ± 2

Question 28

What is anion gap useful in?

Answer 28

differentiating the case of metabolic acidosis

Question 29

common causes of elevated gap?

Answer 29

``` MUDPILES: M: methanol U: uremia D: diabetic ketoacidosis P: Paraldehyde I: Iron, Isoniazid L: lactic acidosis E: ethylene glycol; ethanol, ketoacidosis S: salicylates; starvation ketoacidosis; sepsis ```

Question 30

common causes of non-elevated gap?

Answer 30

``` HARDUP: H: hyperchloremia (parental nutrition) A: acetazolamide R: renal tubular acidosis D: diarrhea U: ureteral diversion P: pancreatic fistula ```

Question 31

question 1 in diagnosis of respiratory/metabolic disturbances and how body compensates

Answer 31

Question 1 What is the osis? As indicated above, look at pH/ If pH <7.35, then its acidosis If pH >7.35, then its alkalosis

Question 32

question 2 in diagnosis of respiratory/metabolic disturbances and how body compensates

Answer 32

2. What is cause of osis? Follow the bicarbonate trail If the answer to question 1 is acidosis then HCO3- is elevated, then RESPIRATORY ACIDOSIS. If the answer to question 1 is acidosis then HCO3- is low, then METABOLIC ACIDOSIS. If the answer to question 1 is alkalosis then HCO3- is low, then RESPIRATORY ALKALOSIS. If the answer to question 1 is alkalosis then HCO3- is elevated, then METABOLIC ALKALOSIS.

Question 33

How do you differentiate acute and chronic respiratory acidosis

Answer 33

acute: 1:0.1 ratio chronic 1:0.35 ratio rise in HCO3- for every 1 mm Hg increase in PaCO2

Question 34

How do you differentiate the metabolic acidosis types?

Answer 34

WInter's equation = expected PaCO2 PaCO2 is within 2, then metabolic acidosis with respiratory compensation. PaCO2 higher than 2, metabolic and respiratory acidosis PaCO2 is low, metabolic acidosis with a respiratory alkalosis

Question 35

How can you differentiate in respiratory alkalosis between acute (uncompensated) and chronic (compensated)?

Answer 35

acute: 1.02 ratio chronic: 1:0.5 ratio

Question 36

What is the metabolic alkalosis equation and what do its results mean?

Answer 36

Expected PaCO2 = (0.7 x rise in HCO3-) + 40 Within 2; metabolic alkalosis with respiratory compensation More than 2; metabolic alkalosis and respiratory acidosis PaCO2 low; metabolic and respiratory alkalosis

Question 37

What graph is used in acid-base disturbances?

Answer 37

Davenport plot

Question 38

Results of CO2 accumulating in the body, which causes an increase in H+ (or decrease in pH) and an increase in HCO3-. Quantitatively in the acute (uncompensated) state, for every 10 mm Hg rise in PaCO2, HCO3- rises about 1 mEq/L and pH falls by 0.08 pH units

Answer 38

respiratory acidosis

Question 39

Respiratory Acidosis can be caused by:

Answer 39

``` Respiratory center depression (anesthetic, morphine) Pulmonary edema, cardiac arrest airway obstruction muscle relaxants sleep apnea chronic obstructive lung disease neuromuscular defects (multiple sclerosis, muscular distrophy) obesity hypoventilation syndrome ```

Question 40

cause and result of respiratory acidosis

Answer 40

Cause: increase in PaCO2 Cause: decrease in pH, slight increase in HCO3-

Question 41

metabolic Acidosis can be caused by:

Answer 41

caused by a gain in fixed (not of CO2 origin) acid and/or a loss of base. The increased H+ drives the reaction to the left, decreasing HCO3- forcing the reaction to the left produces some CO2, but the hyperventilation evoked by the acidosis eliminates CO2.

Question 42

how is metabolic acidosis determined?

Answer 42

Can be determined anion gap MUDPILES for elevated anion gap HARDUP if gap is normal

Question 43

Cause and result of metabolic acidosis?

Answer 43

Cause: gain in H+ as fixed acid and/or a loss of HCO3= (via GI tract or kidney) Result: decrease in pH and HCO3-; compensatory fall in PaCO2

Question 44

Cause of respiratory alkalosis and examples of causes?

Answer 44

``` Caused by an increase in alveolar ventilation relative to body production of CO2 (hyperventilation). Respiratory alkalosis can be caused by: anxiety fever hypoxemia pneumothorax (in some cases) ventilation-perfusion inequality hypotension high altitude ```

Question 45

Cause and result of respiratory alkalosis

Answer 45

Cause: decrease in PaCO2 Result: decrease in H+ (increased pH) and slight decrease in HCO3-

Question 46

What causes metabolic alkalosis and examples

Answer 46

loss of fixed acid and/or gain of base. the decreased H+ forces the reaction to the right, increasing HCO3- Causes: vomiting or gastric suctioning loop and thiazide diuretic use Bartter's, GItelman's, and Liddle's syndrome intracellular shift of hydrogen ions as in hypokalemia primary hyperaldosteronism loss of bicarbonate free fluid (contraction alkalosis)

Question 47

Cause and result of metabolic alkalosis

Answer 47

Cause: loss of H+ and/or gain in HCO-3 Result: increase in pH and HCO3-; compensatory rise in PaCO2

Question 48

equation to compute anion gap

Answer 48

Na+ - (Cl- + HCO3-) | MUDPILES vs HARDUP

Question 49

Graphical depiction of the interplay of pH, HCO3- and PaCO2 as it relates to acid base disorders

Answer 49

Davenport plot

Question 50

ENDOCRINOLOGY

Answer 50

ENDOCRINOLOGY

Question 51

IP3 =

Answer 51

inositol triphosphate

Question 52

DAG =

Answer 52

diacylglycerol

Question 53

Lipid-Soluble Hormones examples

Answer 53

(steroids, thyroid hormones)

Question 54

Water-Soluble Hormones examples

Answer 54

(peptides, proteins)

Question 55

Intracellular actions of Lipid-Soluble Hormones

Answer 55

Stimulates synthesis | of specific new proteins

Question 56

Intracellular actions of Water-Soluble Hormones

Answer 56

Production of second messengers, e.g., cAMP Insulin does not utilize cAMP, instead activates membrane-bound tyrosine kinase Second messengers modify action of intracellular proteins (enzymes)

Question 57

receptors of Lipid-Soluble Hormones

Answer 57

Inside the cell, usually in nucleus

Question 58

receptors of Water-Soluble Hormones

Answer 58

Outer surface of the cell membrane

Question 59

Storage of Lipid-Soluble Hormones

Answer 59

Synthesized as needed Exception: thyroid hormones

Question 60

Storage of Water-Soluble Hormones

Answer 60

Stored in vesicles In some cases, prohor- mone stored in vesicle along with an enzyme that splits off the active hormone

Question 61

Plasma transport of Lipid-Soluble Hormones

Answer 61

Attached to proteins that serve as carriers Exception: adrenal androgens

Question 62

Plasma transport of water-Soluble Hormones

Answer 62

Dissolved in plasma (free, unbound)

Question 63

Half-life of Lipid-Soluble Hormones

Answer 63

Long (hours, days) |  to affinity for protein carrier

Question 64

Half-life of water-Soluble Hormones

Answer 64

Short (minutes) |  to molecular weight

Question 65

The liver produces proteins that bind lipid-soluble hormones, e.g.:

Answer 65

cortisol-binding globulin thyroid-binding globulin sex hormone-binding globulin (SHBG)

Question 66

Liver dysfunction and androgens can decrease and ________ can increase the circulating level of binding proteins.

Answer 66

estrogens For example, a rise in circulating estrogen causes the release of more binding protein by the liver, which binds more free hormone. This explains why during pregnancy and other states with a rise in estrogen levels: Total plasma lipid-soluble hormone increases. Free plasma hormone remains constant at a normal level; thus, the individual does not show signs of hyperfunction.

Question 67

A phenomenon in which one type of hormone must be present before another hormone can act; for example, cortisol must be present for glucagon to carry out gluconeogenesis and prevent hypoglycemia.

Answer 67

Permissive action

Question 68

Thyroid is a fairly constant system and T4 has a half-life of about __________. Thus, a random measurement of total T4 is usually a good estimate of daily plasma levels.

Answer 68

6–7 days

Question 69

Peaks vs nadirs

Answer 69

peaks (erroneous hyperfunction) | nadirs (erroneous hypofunction)

Question 70

Growth hormone is secreted in pulses and mainly at night. This is not reflected in a fasting morning sample. However, growth hormone stimulates the secretion of __________ which circulates attached to protein and has a long half-life (20 hours).

Answer 70

IGF-I Plasma IGF-I measured at any time during the day is usually a good index of overall growth hormone secretion.

Question 71

what does a urinalysis measure?

Answer 71

Restricted to the measurement of catecholamines, steroid hormones, and water-soluble hormones such as hCG and LH.

Question 72

A distinct advantage of urine analysis is that it provides an integrated sample. Example:

Answer 72

A “24-hour urine free cortisol” is often necessary to pick up a low-level Cushing’s syndrome and to eliminate the highs and lows of the normal circadian rhythm.

Question 73

A primary disorder of endocrine system?

Answer 73

A primary disorder means dysfunction originating in the endocrine gland itself, either hyper- or hypo-function.

Question 74

Examples of a primary disorder include:

Answer 74

– excess cortisol from an adrenal adenoma (Conn’s disease) – decreased thyroid secretion (Hashimoto’s thyroiditis) – reduced ADH secretion (central diabetes insipidus)

Question 75

A secondary disorder of endocrine system?

Answer 75

A secondary disorder indicates that a disturbance has occurred causing the gland secrete more or less of the hormone.

Question 76

Examples of a secondary disorder include:

Answer 76

– Cushing disease (pituitary adenoma secreting ACTH) resulting in hypercortisolism – a dehydrated patient with elevated plasma osmolality causing high ADH levels

Question 77

causes of hypofunction of endocrine system

Answer 77

Can be caused by autoimmune disease (e.g., type I diabetes, hypothyroidism, primary adrenal insufficiency, gonadal failure), tumors, hemorrhage, infection, damage by neoplasms

Question 78

hypofunction stimulation test: Hypothalamic hormones test ________

Answer 78

anterior pituitary reserve

Question 79

hypofunction stimulation test: Injection of the pituitary trophic hormone (e.g., ACTH) tests ____________

Answer 79

target gland reserve

Question 80

hypofunction stimulation test: Injection of arginine tests ________________

Answer 80

growth hormone release

Question 81

causes of hyperfunction of endocrine system

Answer 81

Caused by hormone-secreting tumors, hyperplasia, autoimmune stimulation, ectopically produced peptide hormones (e.g., ACTH, ADH)

Question 82

hyperfuntion stimulation tests: Failure of glucose to suppress growth hormone diagnostic for ______

Answer 82

acromegaly

Question 83

hyperfuntion stimulation tests: Failure of dexamethasone (low dose) to suppress cortisol diagnostic for _________

Answer 83

hypercortisolism

Question 84

what is Multiple endocrine neoplasia (MEN) and how does it classify?

Answer 84

Multiple endocrine neoplasia (MEN) represents a group of inheritable syndromes characterized by multiple benign or malignant tumors. o MEN 1: hyperparathyroidism, endocrine pancreas, and pituitary edenomas o MEN 2A: medullary carcinoma of the thyroid, pheochromocytoma, hyperparathyroidism o MEN 2B: medullary carcinoma of the thyroid, pheochromocytoma, hyperparathyroidism typically absent.

Question 85

What is synthesized in neuronal cell bodies in the arcuate and paraventricular nuclei?

Answer 85

``` hypothalamic hormones thyrotropin-releasing hormone (TRH) corticotropin-releasing hormone (CRH) growth hormone–releasing hormone (GHRH) somatostatin (SST) dopamine ```

Question 86

What is synthesized in the preoptic nucleus?

Answer 86

gonadotropin-releasing hormone (GnRH)

Question 87

TRH

Answer 87

thyrotropin-releasing hormone

Question 88

TSH

Answer 88

thyroid-stimulating hormone or thyrotropin

Question 89

CRH

Answer 89

corticotropin-releasing hormone

Question 90

ACTH

Answer 90

adrenocorticotropic hormone or corticotropin

Question 91

GnRH

Answer 91

gonadotropin-releasing hormone

Question 92

LH

Answer 92

luteinizing hormone

Question 93

FSH

Answer 93

follicle-stimulating hormone

Question 94

GHRH

Answer 94

growth hormone–releasing hormone

Question 95

GH

Answer 95

growth hormone

Question 96

SST

Answer 96

somatostatin

Question 97

Characteristic sequential loss of function of hypothyroidism

Answer 97

growth hormone and gonadotropin, followed by TSH then ACTH and finally prolactin.

Question 98

Kallman syndrome – (tertiary) defective:

Answer 98

GnRH synthesis; ↓ LH ↓ FSH ↓ sex steroids

Question 99

_________ is the most common tumor affecting the hypothalamic–pituitary system in children (pituitary adenomas rare).

Answer 99

Craniopharyngioma

Question 100

The pituitary in pregnancy is enlarged and therefore more vulnerable to infarction. Sometimes when delivery is associated with severe blood loss, the ensuing shock causes arteriolar spasm in the pituitary with subsequent ischemic necrosis. Some degree of hypopituitarism has been reported in 32% of women with severe postpartum hemorrhage. Symptoms vary, depending on the extent and location of pituitary damage, but failure to lactate for days following birth is a strong sign of pituitary damage.

Answer 100

Sheehan syndrome

Question 101

Pulsatile system and the pulsatile release of GnRH prevents downregulation of ________ receptors.

Answer 101

gonadotroph receptors

Question 102

What is mass effect?

Answer 102

The mass effect causes sequential loss of GH and gonadotropin followed by TSH, ACTH, and finally prolactin.

Question 103

What is the most common tumor and the most common manifestation?

Answer 103

Prolactinomas are the most common tumor, and hypogonadism is the most common manifestation.

Question 104

what are the Secreted hormones of the posterior pituitary gland?

Answer 104

arginine vasopressin (ADH), oxytocin — both are peptide hormones.

Question 105

ADH function

Answer 105

ADH is a major controller of water excretion and regulator of extracellular osmolarity.

Question 106

what can stimulate ADH secretion?

Answer 106

Angiotensin II and CRH can stimulate the release of ADH.

Question 107

Neural control mechanisms that regulate secretion of ADH by the posterior pituitary. The principal inputs are inhibition by:

Answer 107

Baroreceptor and cardiopulmonary mechanoreceptors and stimulation by osmoreceptors.

Question 108

Synthesis of ADH?

Answer 108

the supraoptic (SO) and paraventricular (PVN) nuclei of the hypothalamus

Question 109

Storage and releases ADH?

Answer 109

Posterior pituitary

Question 110

What are Osmoreceptors?

Answer 110

Osmoreceptors are neurons that respond to increased plasma osmolarity, principally plasma sodium concentration. They synapse with neurons of the SO and PVN and stimulate them to secrete ADH from the posterior pituitary. They also stimulate consumption of water through hypothalamic centers that regulate thirst.

Question 111

SO and PVN also receive inputs from where?

Answer 111

The SO and PVN also receive input from cardiopulmonary mechano- receptors, as well as arterial baroreceptors. High blood volume or blood pressure tends to inhibit secretion of ADH.

Question 112

main target tissue of ADH

Answer 112

The main target tissue is the renal collecting duct (V2 receptors).

Question 113

Actions of ADH?

Answer 113

ADH increases the permeability of the duct to water by placing water channels (aquaporins) in the luminal membrane. ADH, acting via the V1 receptor, contracts vascular smooth muscle.

Question 114

What is Atrial Natriuretic Peptide (ANP)?

Answer 114

ANP is the hormone secreted by the heart. ANP is found throughout the heart but mainly in the right atrium. The stimuli that release ANP (two peptides are released) are: Stretch, an action independent of nervous involvement CHF and all fluid overload states

Question 115

ANP function in kidneys

Answer 115

ANP also increases sodium loss (natriuresis) and water loss (diuresis) by the kidney because it inhibits aldosterone release as well as the reabsorption of sodium and water in the collecting duct.

Question 116

The consequences of Diabetes Insipidus can be explained on the basis of the lack of an effect of ________

Answer 116

ADH on the renal collecting ducts.

Question 117

Sufficient ADH is not available to affect the renal collecting ducts. Causes include familial, tumors (craniopharyngioma), autoimmune, trauma Pituitary trauma – transient diabetes insipidus Sectioning of pituitary stalk – triphasic response: diabetes insipidus, fol- lowed by SIADH, followed by a return of diabetes insipidus Destruction of the hypothalamus from any cause can lead to diabetes insipidus. Forms of hypothalamic destruction are stroke, hypoxia, head trauma, infection, cancer or mass lesions. CDI = ADH deficiency. CDI is treated with replacing ADH as vasopressin or DDAVP (desmopressin).

Answer 117

Central diabetes insipidus (CDI)

Question 118

Due to inability of the kidneys to respond to ADH l Causes include familial, acquired, drugs (lithium) l Hypokalemia Hypercalcemia

Answer 118

Nephrogenic diabetes insipidus

Question 119

What is able to diminish ADH’s effectiveness on principal cells?

Answer 119

Lithium, low potassium, and high calcium

Question 120

Excessive secretion of ADH causes an inappropriate increased reabsorption of water in the renal collecting duct.

Answer 120

Syndrome of Inappropriate ADH Secretion (SIADH)

Question 121

causes of SIADH

Answer 121

Ectopic production of ADH (any CNS or small cell lung pathology) Drug induced: SSRI, carbamazepine Lesions in the pathway of the baroreceptor system

Question 122

Pathophysiology of SIADH

Answer 122

Increased water retention, hyponatremia, but clinically euvolumic Inappropriate concentration of urine, often greater than plasma osmolarity With hyponatremia, a normal person should have urine sodium and osmolarity that are low. In SIADH, it is a disease because urine sodium and osmolarity are inappropriately high.

Question 123

Treatment of SIADH

Answer 123

Fluid restriction but not salt restriction Sodium disorders cause neurological symptoms. Only mild hyponatremia from SIADH can be managed with fluid restriction. Severe disease needs 3% hypertonic saline or V2 receptor antagonists. Conivaptan and tolvaptan are V2 receptor antagonists; they stop ADH effect on kidney tubule.

Question 124

One of the most common disorders of fluid and electrolyte balance in hospitalized patients Is usually equivalent to a hypo-osmolar state (exception hyperglycemia) l Involves both solute depletion and water retention but water retention is usually the more important factor Solute depletion can occur from any significant loss of ECF fluid. The hyponatremia is the result of replacement by more hypotonic fluids. When it develops rapidly (< 48 hours) and is severe (Na < 120 mEq/L), patient is at risk for seizures and respiratory arrest. Often treated aggres- sively with hypertonic saline (3%) and diuretics or ADH antagonists. When it develops more slowly, it appears to be well-tolerated and patient is asymptomatic. Aggressive treatment may result in “central pontine myelinolysis.” General recommendation is to slowly raise Na concentration over a period of days.

Answer 124

HYPONATREMIA

Question 125

Caused by marked reduction in water excretion and/or increased rate of water ingestion. Would include congestive heart failure and cirrhosis

Answer 125

Hypervolemia

Question 126

Indicates solute depletion. Would include mineralocorticoid de ciency, diuretic abuse, renal disease, diarrhea, and hemorrhage

Answer 126

Hypovolemia

Question 127

Would include SIADH and primary (psychogenic) polydipsia. A clinically equiv- alent presentation may occur in glucocorticoid de ciency or hypothyroidism.

Answer 127

Clinical euvolemia

Question 128

The major action of ADH is the reabsorption of _____ and _____, but not electrolytes, in the renal collecting duct.

Answer 128

water | urea

Question 129

ANP, found mainly in the tissue of the right atrium, is released in response to stretch. The major action of ANP is ______ and ______.

Answer 129

diuresis | natriuresis

Question 130

what is SIADH?

Answer 130

Inappropriately elevated secretion of ADH. Characterized by euvolemia but hyponatremia.

Question 131

ADRENAL CORTEX

Answer 131

ADRENAL CORTEX

Question 132

________ controls the release of both cortisol and adrenal androgens.

Answer 132

ACTH

Question 133

_______ is stimulated by a rise in angiotensin II and/or K+.

Answer 133

Aldosterone

Question 134

Zona Aldosterone of adrenal gland. Hormone: Controlled by:

Answer 134

Angiotensin II [K+]

Question 135

Zona fasciculata of adrenal gland. Hormone: Controlled by:

Answer 135

Cortisol ACTH

Question 136

Zona reticularis of adrenal gland Hormone: Controlled by:

Answer 136

Androgens ACTH

Question 137

Medulla of adrenal gland Hormone: Controlled by:

Answer 137

Epinephrine Autonomic nervous system

Question 138

T/F: LH has no effect on the production of adrenal androgens

Answer 138

TRUE

Question 139

HSD =

Answer 139

hydroxysteroid dehydrogenase

Question 140

OH =

Answer 140

Hydroxylase

Question 141

In females and prepubertal males, urinary 17-ketosteroids are an index of ____________. l In adult males (postpuberty), urinary 17-ketosteroids are 2/3 adrenal and 1/3 testicular, and thus mainly an index of ____________.

Answer 141

adrenal androgen secretion. adrenal secretion

Question 142

_______ converts androgen into estrogen.

Answer 142

Aromatase

Question 143

e starting point in the synthesis of all steroid hormones is the transport of cholesterol into the mitochondria by __________. This is is the rate-limiting step.

Answer 143

steroidogenic acute regulatory protein (StAR)

Question 144

The enzyme catalyzing the conversion of cholesterol to pregnenolone is ___________

Answer 144

side-chain cleavage enzyme (SCC, also called desmolase.).

Question 145

Angiotensin II is the main stimulus to the zona glomerulosa, which produces ______, the major mineralocorticoid.

Answer 145

aldosterone

Question 146

_________: Main glucocorticoid secreted by the adrenal cortex, responsible for most of the hypothalamic and anterior pituitary negative feedback control of ACTH secretion.

Answer 146

Cortisol

Question 147

Normal hormonal output of the zona reticularis consists of the following: _______: These weak water-soluble androgens represent a sig- nificant secretion; however, they produce masculinizing characteristics only in women and prepubertal males when secretion is excessive.

Answer 147

Adrenal androgens

Question 148

Stress hormones usually act to mobilize energy stores. The stress hormones are: _______ : mobilizes fatty acids by increasing lipolysis in adipose tissue _______ : mobilizes glucose by increasing liver glycogenolysis _____ : mobilizes fat, protein, carbohydrate ______, in some forms of stress such as exercise: mobilizes glucose via glycogenolysis and fat via lipolysis

Answer 148

Growth hormone Glucagon Cortisol Epinephrine

Question 149

Metabolic Actions of _______: It promotes the mobilization of energy stores, speci cally: Protein: It promotes degradation and increased delivery of hepatic gluconeogenic precursors. Lipids: It promotes lipolysis and increased delivery of free fatty acids and glycerol. Carbohydrate: Cortisol raises blood glucose, making more glucose available for nervous tissue. Two mechanisms are involved: – It counteracts insulin’s action in most tissues (muscle, lymphoid, and fat). – It increases hepatic output of glucose by regulating the enzymes involved in gluconeogenesis, particularly phosphoenolpyruvate carboxykinase (PEPCK) (not from liver glycogenolysis).

Answer 149

Cortisol

Question 150

what does cortisol do with glucagon?

Answer 150

Promotes glycogenolysis in the liver (some lipolysis from adipocytes as well). Without cortisol, fasting hypoglycemia rapidly develops. Cortisol permits gluca- gon to raise blood glucose.

Question 151

What does cortisol do with Catecholamines?

Answer 151

Promotes both alpha and beta receptor expression. Beta receptor function involves glucose regulation, lipolysis, and bronchodilation. Alpha receptor function is pivotal for blood pressure regulation. Without cortisol, blood pressure decreases.

Question 152

Secretion of CRH increases in response to stress and in the early morning. What are the hours?

Answer 152

Peak cortisol secretion occurs early in the morning between the 6th and 8th hours of sleep. Secretion then declines slowly during the day and reaches a low point late in the evening.

Question 153

CRN + cortisol relationship

Answer 153

Increased AM CRH = increased AM cortisol Increased AM cortisol = increased AM blood sugar and lipid levels Increased AM sugar and lipid levels help get you out of bed

Question 154

what stimulates the release of the secretion of cortisol (and adrenal androgens) of adrenal cortex?

Answer 154

ACTH

Question 155

__________ suppresses the release of ACTH by acting on the hypothalamus and anterior pituitary.

Answer 155

Cortisol

Question 156

What causes darkening of the skin in relation to hormones?

Answer 156

Excessive secretion of ACTH (e.g., primary adrenal insuciency) causes darkening of the skin. Its is due to the melanocyte-stimulating hormone (α-MSH) sequence within the ACTH molecule, and the β-MSH activity of β-lipotropin.

Question 157

role of β-Lipotropin?

Answer 157

Role not well understood Precursor to β-MSH and endorphins. Endorphins modulate the percep- tion of pain.

Question 158

primary target tissue for aldosterone and its function?

Answer 158

The primary target tissue for aldosterone is the kidney, where it increases Na+ reabsorption by the principal cells of the kidney’s collecting ducts. Because water is reabsorbed along with the Na+, aldosterone can be considered to control the amount of Na+ rather than the concentration of Na+ in the ECF. Aldosterone also promotes the secretion of H+ by the intercalated cells of the col- lecting duct, and K+ secretion by the principal cells. The Na+-conserving action of aldosterone is also seen in salivary ducts, sweat glands, and the distal colon.

Question 159

_________ promotes the activity of Na/K-ATPase–dependent pump that moves Na+ into the renal ECF in exchange for K+. In addition, it also enhances epithelial Na+ channels (ENaC) in the luminal membrane of principal cells. The net effect is to increase Na+ reabsorption, which in turn increases water reabsorption. It regulates Na+ to regulate extracellular volume.

Answer 159

Aldosterone

Question 160

Acutely, ACTH increases aldosterone secretion. However, the primary regulators of aldosterone secretion are circulating levels of _____ and _____.

Answer 160

Ang II and K+

Question 161

What are the main sensory cells of the afferent arteriole?

Answer 161

The main sensory cells are the granular cells (also called juxtamedullary cells) of the afferent arteriole. They are modified smooth-muscle cells that surround and directly monitor the pressure in the afferent arteriole. This signal in many cases is in response to a reduction in circulating fluid volume. These cells are also innervated and stimulated by sympathetic neurons via norepinephrine and beta receptors. Thus the release of renin induced by hypovolemia is enhanced by increased sympathetic neural activity.

Question 162

Long-term regulation of blood pressure and cardiac output is accomplished by the ____________.

Answer 162

renin-angiotensin-aldosterone system

Question 163

what does renin do?

Answer 163

Renin is an enzyme that converts a circulating protein produced in the liver, angiotensinogen into angiotensin I

Question 164

What does ACE do?

Answer 164

Angiotensin converting enzyme (ACE), found mainly in endothelial cells of pulmonary vessels, converts angiotensin I into angiotensin II.

Question 165

what does Angiotensin II do?

Answer 165

Angiotensin II has potent ef- fects to stimulate secretion of aldosterone and to cause arteriolar vasoconstric- tion. It also directly stimulates reabsorption of sodium in the proximal tubule

Question 166

How does Angiotensin II raises blood pressure?

Answer 166

Angiotensin II raises blood pressure by 2 independent actions: The direct vasoconstrictive effects of angiotensin II increase total peripheral resistance. It stimulates the adrenal cortex to secrete aldosterone, resulting in increased reabsorption of Na+.

Question 167

In addition to its effects to serve as a direct vasoconstrictor and increase aldosterone secretion, angiotensin II also:

Answer 167

- Increases ADH release from posterior pituitary - Increases thirst - Increases sodium reabsorption in proximal tubule

Question 168

There is hypercortisolism regardless of origin, including chronic glucocorticoid therapy

Answer 168

Cushing syndrome

Question 169

It is hypercortisolism due to an adenoma of the anterior pituitary (microadenoma)

Answer 169

Cushing disease

Question 170

what is 1-mg overnight dexamethasone suppression test used for?

Answer 170

For the presence of Cushing syndrome regardless of the cause Normal; cortisol decreases Hypercortisolism; cortisol not suppressed False-positives from depression or alcoholism

Question 171

what is High-dose dexamethasone used for?

Answer 171

To differentiate pituitary adenoma from ectopic ACTH secretion and adrenal tumors Pituitary source; cortisol decreases Ectopic ACTH, adrenal tumor; cortisol not suppressed

Question 172

ACTH level tests used for? what do its results mean?

Answer 172

Used after 24 hour urine cortisol establishes presence of hypercortisolism ACTH levels establish etiology of hypercortsolism Low ACTH = Adrenal source of cortisol overproduction Normal or high ACTH = Pituitary or Ectopic source High dose dexamethasone distinguishes Pituitary vs Ectopic source

Question 173

ACTH stimulation test diagnoses _______. To diagnose atrophied adrenal nonresponsive Normal; cortisol increases after ACTH Adrenal insufficiency: no change in cortisol level

Answer 173

adrenal insufficiency.

Question 174

T/F: Metyrapone testing is no longer performed.

Answer 174

TRUE

Question 175

What is this: ACTH independent Cortisol elevated, ACTH depressed Most are benign adrenocorticol adenomas Adrenal adenoma usually unilateral and secretes only cortisol; decreased adrenal androgen and deoxycorticosterone (hirsutism absent) Presence of androgen or mineralocorticoid excess suggests a carcinoma

Answer 175

Primary hypercortisolism (adrenal source)

Question 176

What is this: ACTH dependent Hypersecretion of ACTH results in bilateral hyperplasia of the adrenal zona fasciculata and reticularis Elevated ACTH, cortisol, adrenal androgen, deoxycorticosterone

Answer 176

Secondary hypercortisolism (pituitary vs. ectopic source)

Question 177

What are the Two main subcategories of Secondary hypercortisolism?

Answer 177

Pituitary adenoma | Ectopic ACTH syndrome

Question 178

- Usually a microadenoma (< 1 cm dia.) - This is Cushing disease - Increased ACTH not sufficient to cause hyperpigmentation - Dexamethasone suppressible

Answer 178

Pituitary adenoma

Question 179

- Most frequently in patients with small cell carcinoma of the lung - Greater secretion of ACTH than in Cushing disease and hyperpigmentation often present - Ectopic site nonsupressible with dexamethasone

Answer 179

Ectopic ACTH syndrome

Question 180

High-dose dexamethasone – ACTH suppressed = – ACTH not suppressed =

Answer 180

– ACTH suppressed = Cushing disease (pituitary source) | – ACTH not suppressed = ectopic ACTH syndrome

Question 181

What is this: - Obesity because of hyperphagia, classically central affecting mainly the face, neck, trunk, and abdomen: “moon facies” and “buffalo hump” - Protein depletion as a result of excessive protein catabolism - Inhibition of inflammatory response and poor wound healing - Hyperglycemia leads to hyperinsulinemia and insulin resistance. l Hyperlipidemia - Bone breakdown and osteoporosis - Thinning of the skin with wide purple striae located around abdomen and hips - Increased adrenal androgens, when present in women, can result in acne, mild hirsutism, and amenorrhea. - In men, decreased libido and impotence - Mineralocorticoid effects of the high level of glucocorticoid and deoxycorticosteroid lead to salt and water retention (hypertension), potassium depletion, and a hypokalemic alkalosis. - Increased thirst and polyuria - Anxiety, depression, and other emotional disorders may be present.

Answer 181

Characteristics of Cushing Syndrome

Question 182

What is this: - Autoimmune origin with slow onset in about 80% of cases - Loss of 90% of both adrenals required before obvious clinical manifestations - With gradual adrenal destruction, basal secretion is normal but secretion does not respond to stress, which may initiate an adrenal crisis. - Bilateral hemorrhage as the origin results in an adrenal crisis. Hyperpigmentation, hyponatremia, and hyperkalemia usually absent - Orthostatic intolerance due to diminished alpha-receptor function and low blood volume. - Abnormalities in GI function - Loss of axillary and pubic hair in women due to loss of androgens, amenorrhea - Insufficient glucocorticoids leads to hypoglycemia and an inability of the kidney to excrete a water load - Severe hypoglycemia in children but rare in adults

Answer 182

Primary Hypocortisolism (in primary adrenal insufficiency, Addison’s disease)

Question 183

What is this: - Most commonly due to sudden withdrawal of exogenous glucocorticoid therapy - Trauma, infection, and infarction most common natural origin of ACTH deficiency - In the early stages baseline hormone values are normal but ACTH reserve compromised and stress response subnormal (glucocorticoids adminis- tered presurgery) - May be associated with the loss of other anterior pituitary hormones (pan- hypopituitarism) or adenomas secreting prolactin or growth hormone - Atrophy of the zona fasciculata and zona reticularis - Zona glomerulosa and aldosterone normal; no manifestations of mineralocorticoid deficiency - Consequences as stated for cortisol deficiency - Severe hypoglycemia and severe hypotension unusual (RAAS is still intact) - Hyponatremia due to water retention

Answer 183

Secondary hypocortisolism (secondary adrenal insufficiency)

Question 184

What is this: - Most common cause is a small unilateral adenoma, on either side - Remainder mostly bilateral adrenal hyperplasia (idiopathic hyperaldosteronism) - Rarely due to adrenal carcinoma - Increased whole body sodium, fluid, and circulating blood volume - Hypernatremia is infrequent. - Increased peripheral vasoconstriction and TPR - Blood pressure from borderline to severe hypertension - Edema rare (sodium escape*) - Modest left ventricular hypertrophy - Potassium depletion and hypokalemia create symptoms of weakness and fatigue. - Detection of hypertension with hypokalemia is often the initial clue for this disease - Increased hydrogen ion excretion and new bicarbonate create metabolic alkalosis. - A positive Chvostek or Trousseau’s sign is suggestive of alkalosis leading to low calcium levels. - Cortisol is normal. - Suppression of renin a major feature

Answer 184

Primary hyperaldosteronism (Conn’s syndrome)

Question 185

What is this: - In most cases a primary over-secretion of renin secondary to a decrease in renal blood flow and/or pressure - Renal arterial stenosis, narrowing via atherosclerosis, fibromuscular hyperplasia. - Renin-secreting tumor rare - Modest to highly elevated renin - Modest to highly elevated aldosterone - Hypokalemia and metabolic alkalosis

Answer 185

Secondary hyperaldosteronism with hypertension

Question 186

What is this: Sequestration of blood on the venous side of the systemic circulation is a common cause of ______. This results in decreased cardiac output and thus decreased blood flow and pressure in the renal artery. The following conditions produce this disease through this mechanism: - Congestive heart failure - Constriction of the vena cava - Hepatic cirrhosis

Answer 186

Secondary hyperaldosteronism with hypotension

Question 187

This type of deficiency is the most common of the congenital enzyme deficiencies. Tissues affected: zona glomerulosa, zona fasciculata, zona reticularis

Answer 187

21 β-hydroxylase deficiency

Question 188

what does this mean? 21 β-OH

Answer 188

21 β-Hydroxylase blockade

Question 189

Consequence of 21 β-OH?

Answer 189

Consequence: Result is a decreased production of aldosterone, the main miner- alocorticoid.

Question 190

What does a 17 α-Hydroxylase blockade point do in the testes?

Answer 190

Decreased production of all androgens including testosterone

Question 191

What does a 17 α-Hydroxylase blockade point do in the testes?

Answer 191

Decreased production of estrogens and androgens

Question 192

What is this? - Accounts for about 90% of the cases - 75% of the cases have mineralocorticoid deficiency - Neonates may present with a salt-wasting crisis. - Salt wasters tend to have hyponatremia, hyperkalemia, and raised plasma renin. - 17-hydroxyprogesterone is elevated. - Increased androgens lead to virilization of the female fetus and sexual ambiguity at birth - Males are phenotypically normal at birth but develop precocious pseudopuberty, growth acceleration, premature epiphyseal plate closure, and diminished final height. - Goal in treatment is to bring glucocorticoid and mineralocorticoid back to the normal range which would also suppress adrenal androgen secretion. - Give hydrocortisone to act as feedback inhibition on pituitary.

Answer 192

21 β-Hydroxylase deficiency

Question 193

What is this? - Extremely rare - Usually diagnosed at the time of puberty when the patient presents with hypertension, hypokalemia, and hypogonadism - Individuals have eunuchoid characteristics.

Answer 193

17 α-Hydroxytlase deficiency

Question 194

In ________ β-hydroxylase deficiency, there is mineralocorticoid de ciency, salt wasting and hypotension, androgen excess and female virilization.

Answer 194

21 β-hydroxylase deficiency

Question 195

In _______ β-hydroxylase deficiency, there is mineralocorticoid excess, salt retention and hypertension, androgen excess as in the preceding.

Answer 195

11 β-hydroxylase deficiency

Question 196

In 17 α-hydroxylase deficiency, there is mineralocorticoid excess, adrenal androgen de ciency, and hypertension with gonadal steroid de ciency and hypogonadism.

Answer 196

17 β-hydroxylase deficiency

Question 197

ADRENAL MEDULLA

Answer 197

ADRENAL MEDULLA

Question 198

what does the adrenal medulla secrete?

Answer 198

Secretion of the adrenal medulla is 20% norepinephrine and 80% epinephrine.

Question 199

what converts norepinephrine into epinephrine?

Answer 199

Phenylethanolamine-N-methyltransferase (PMNT) converts norepinephrine into epinephrine.

Question 200

Most circulating norepinephrine arises from _____.

Answer 200

postganglionic sympathetic neurons

Question 201

T/F: Because many of the actions of epinephrine are also mediated by norepinephrine, the adrenal medulla is not essential for life.

Answer 201

TRUE

Question 202

what kind of people suffer from orthostatic hypotension?

Answer 202

The vasoconstrictive action of norepinephrine is essential for the maintenance of normal blood pressure, especially when an individual is standing. Plasma norepinephrine levels double when one goes from a lying to a standing position. People with inadequate production of norepinephrine suffer from orthostatic hypotension.

Question 203

when does Epinephrine increase?

Answer 203

Epinephrine is a stress hormone and rapidly increases in response to exercise, exposure to cold, emergencies, and hypoglycemia.

Question 204

metabolic function of Epinephrine in liver.

Answer 204

Liver: Epinephrine increases the activity of liver and muscle phosphorylase, promoting glycogenolysis. This increases glucose output by the liver.

Question 205

metabolic function of Epinephrine in Skeletal muscle.

Answer 205

Skeletal muscle: Epinephrine promotes glycogenolysis but because muscle lacks glucose-6-phosphatase, glucose cannot be released by skeletal muscle; instead, it must be metabolized at least to lactate before being released into the circulation.

Question 206

metabolic function of Epinephrine in Adipose tissue.

Answer 206

Adipose tissue: Epinephrine increases lipolysis in adipose tissue by increasing the activity of hormone-sensitive lipase. Glycerol from TG breakdown is a minor substrate for gluconeogenesis.

Question 207

metabolic function of Epinephrine in metabolic rate

Answer 207

Epinephrine increases the metabolic rate. This will not occur without thyroid hormones or the adrenal cortex.

Question 208

what is this: - Adrenal tumors that secrete epinephrine and norepinephrine in various ratios - Usually unilateral benign tumors - Characteristic of MEN 2A and MEN 2B - Paragangliomas are extra-adrenal pheochromocytomas of sympathetic ganglia located primarily within the abdomen and that secrete norepinephrine. - Most consistent feature is hypertension. Symptoms include headache, diaphoresis, palpitations, and anxiety. -Increased metabolic rate and hyperglycemia also occur. - Pheochromocytomas are highly vascular and encapsulated. - Episodic release of hormone, particularly when it is mainly norepinephrine, can abruptly cause a hypertensive crisis. Can be induced by physical stimuli that displaces abdominal contents. - Most reliable initial test is plasma metanephrines or 24-hour urine cat- echolamines or metanephines. - Usually curable but can be fatal if undiagnosed - Treat with alpha blocker followed by surgical removal.

Answer 208

pheochromocytoma

Question 209

The most reliable test of Epinephrine?

Answer 209

urine metanephrines.

Question 210

ENDOCRINE PANCREAS

Answer 210

ENDOCRINE PANCREAS

Question 211

Delta cells, which constitute about 5% of the islet cells, are interspersed between the alpha and beta cells and secrete ________.

Answer 211

somatostatin

Question 212

Alpha cells, which constitute about 20% of the islet cells, secrete ______ and tend to be located near the periphery of the islet.

Answer 212

glucagon

Question 213

Beta cells constitute 60–75% of the islet cells. Beta cells synthesize preproinsulin, which is cleaved to form proinsulin, which, in turn, splits into _______ and _____ both of which are secreted in equimolar quantities.

Answer 213

insulin and C peptide

Question 214

what is the long-term marker of endogenous insulin secretion

Answer 214

C-peptide For many years, C-peptide was considered to have no biological function, but more recently this has been called into question. Studies suggest that C-peptide receptors exist on cells. In addition, C-peptide may serve a protective role, helping to prevent the renal, neural, and microvascular pathologies seen when it is absent, i.e., type I diabetes mellitus.

Question 215

-insulin receptor- - The portion of the insulin receptor that faces externally has the ___________. - The portion of the insulin receptor that faces the cytosol has _________ activity. When occupied by insulin, the receptor phosphorylates itself and other proteins.

Answer 215

hormone-binding domain tyrosine kinase activity

Question 216

The most important controller of insulin secretion is _____. Above a threshold of 100 mg%, insulin secretion is directly proportional to it.

Answer 216

plasma glucose

Question 217

Glucagon is a peptide hormone. It is secreted by the _______ of the pancreatic islets.

Answer 217

α-cells of the pancreatic islet

Question 218

The primary target for glucagon action is the _______, where its action is mediated by an increase in the concentration of cAMP. The cAMP activates protein kinase A, which, by catalyzing phosphorylation, alters the activity of enzymes mediating the actions given below.

Answer 218

liver hepatocyte

Question 219

T/F: Skeletal muscle is a target tissue for glucagon.

Answer 219

FALSE

Question 220

What is this: ``` Increases liver glycogenolysis. Increases liver gluconeogenesis. Increases liver ketogenesis and decreases lipogenesis. Increases ureagenesis. Increases insulin secretion. Increases lipolysis in the liver. ```

Answer 220

Specific Actions of Glucagon on the Liver

Question 221

Stimuli that inhibit glucagon secretion

Answer 221

Hyperglycemia Insulin Somatostatin

Question 222

Stimuli that promote glucagon secretion

Answer 222

Hypoglycemia | Amino acids arginine

Question 223

most important physiologic promoter for glucagon secretion and the most important inhibitor?

Answer 223

Low plasma glucose (hypoglycemia) is the most important physiologic promoter for glucagon secretion, and elevated plasma glucose (hyperglycemia) the most important inhibitor.

Question 224

Amino acids, especially _________, also promote the secretion of glucagon. us, glucagon is secreted in response to the ingestion of a meal rich in proteins.

Answer 224

dibasic amino acids (arginine, lysine)

Question 225

- Accounts for about 90% of all the cases of diabetes - Strong genetic component - Body build is usually obese (particularly central or visceral). - Usually, but not always, middle-aged or older - The number of younger individuals in this category is increasing. - Characterized by variable degrees of insulin resistance, impaired insulin secretion, and increased hepatic output of glucose. Insulin resistance precedes secretory defects and in the early stages hyperinsulinemia is able to overcome tissue resistance. Ultimately beta cell failure can occur. - Insulin levels may be high, normal, or low. - Resistance to insulin is not well understood. It is thought to be due to postreceptor defects in signaling, which ultimately lead to a decrease in the number of glucose transporters. Reducing plasma glucose and thus plasma insulin can increase receptor sensitivity toward normal. - Plasma glucose good screening for type 2. Elevated glucose due to elevated hepatic output. - With a controlled diet and exercise, the symptoms of type 2 diabetes often disappear without the necessity for pharmacologic therapy. - Individuals tend to be ketosis resistant. The presence of some endogenous insulin secretion appears to protect from development of a ketoacidosis. If it does develop, it is usually the result of severe stress or infection (increased counterregulatory homones, suppressed insulin). - In nonobese patients, a deficient insulin release by the pancreas is often the problem, but varying degrees of insulin resistance can also occur.

Answer 225

type 2 diabetics

Question 226

A group of metabolic derangements that includes atherogenic dyslipidemia (low HDL) and high triglycerides, elevated blood glucose, hypertension, central obesity, prothrombotic state, and a proinflammatory state. The clustering of these risk factors increases the probability of developing cardiovascular disease and type 2 diabetes.

Answer 226

Metabolic Syndrome (Syndrome X)

Question 227

- Genetic association less marked than the other type - Genetically predisposed individuals whose immune system destroys pancreatic beta cells - Symptoms do not become evident until 80% of the beta cells are destroyed. l Body build usually lean - Usually, but not always, early age of onset - Due to an absence of insulin production - Increased glucagon secretion also generally occurs - Three target tissues for insulin—liver, skeletal muscle, and adipose tissue—fail to take up absorbed nutrients (glucose, amino acids, and fatty acids), thus increasing their levels in the blood.

Answer 227

diabetes mellitus type 1

Question 228

What is this: - Without any insulin, excessive lipolysis provides fatty acids to the liver, where they preferentially converted to ketone bodies because of the unopposed action of glucagon. - Blood pH and bicarbonate decrease due to the metabolic acidosis. - Increased alveolar ventilation is the respiratory compensation for the metabolic acidosis. When the arterial pH decreases to about 7.20, ventilation becomes deep and rapid (Kussmaul breathing). - An acidic urine results as the kidneys attempt to compensate for the acidosis. - The severe acidosis is in addition to the dehydration and net decrease in total body sodium and potassium. - Treatment is replacement of fluid and electrolytes and administration of insulin - DKA treatment is first 2-3 liters of normal saline and IV insulin. Subcutaneous insulin may not be fully absorbed because of decreased skin perfusion. Hyponatremia is common because of hyperglycemia. For each 100 point increase in glucose above normal, there is a 1.6 decrease in sodium. - When hyponatremia is present with hyperglycemia, management is cor- rection of the elevated glucose level. When glucose comes to normal, the sodium corrects.

Answer 228

Diabetic Ketoacidosis (DKA)

Question 229

What is the ratio in Diabetic Ketoacidosis (DKA)?

Answer 229

100 mg ELEVATION glucose = 1.6 meq DECREASE sodium

Question 230

What is this: - Most common islet cell tumor - Found almost exclusively within the pancreas and hypersecrete insulin - Most common symptoms due to the hypoglycemia (confusion, disorienta- tion, headache) - Association with MEN 1 - Insulin measured to determine insulin-mediated versus noninsulin-mediated hypoglycemia - Insulin-secreting tumor: insulin and C-peptide both elevated l Factitious hypoglycemia: C-peptide below normal - Treat with removal

Answer 230

Insulinomas

Question 231

Which hormone is this: - It is produced in adipose tissue and is thought to be a “long-term” regulator of appetite and energy balance. - Secretion is circadian, with the highest levels occurring at night and the nadir in the morning. Individual meals do not stimulate the release of it. - Its receptor is a member of the cytokine family of receptors, which activate gene transcription factors. - It decreases hypothalamic neuropeptide Y (NPY), which is a potent activator of feeding (orexigenic). By inhibiting NPY synthesis, it promotes satiety (anorexigenic). - It increases energy expenditure, in part by increasing fatty acid oxidation, and it decreases fat stores. - Lack of and/or resistance to it causes obesity.

Answer 231

Leptin

Question 232

Which hormone is this: - It is produced in adipose tissue, and it increases insulin sensitivity and tissue fat oxidation. - Dysregulation of adiponectin, along with production of cytokines by adipocytes, may play a role in obesity, insulin resistance, and cachexia. -----Plasma levels of it are low in Type II diabetics, and infusion of this hormone decreases plasma glucose in experimental animal models of diabetes mellitus. - The mechanism of action and regulation of secretion are not well understood, but it does appear to inhibit liver output of glucose.

Answer 232

adiponectin

Question 233

Which hormone is this: - It is produced by cells of the stomach. - Circulating levels of ghrelin are reduced in response to a meal and highest in the fasting state. - It activates hypothalamic NYP neurons and is thus a potent orexigenic hormone. - It also stimulates the release of growth hormone (GH), although its physiologic significance/ role is not well understood. Because of ghrelin’s effects on GH and appetite, however, it may prove beneficial for restoring GH levels in the elderly and anorexic conditions, such as cancer. - It levels are decreased in obese individuals and elevated by low calorie diets, strenuous exercise, and patients with Prader-Willi syndrome. - Ghrelin is a peptide hormone that works via Gq and Gs. Its mechanism of action and regulation of secretion are not well understood.

Answer 233

Ghrelin

Question 234

``` Administration of the ________ class of compounds to diabetics increases the circulating levels of adiponectin, which may be part of the mechanism by which these drugs reduce plasma glucose. ```

Answer 234

thiazolidinedione (TZD)

Question 235

_______ is a genetic condition affecting many parts of the body. In infancy, this condition is characterized by hypotonia, feeding dif culties, poor growth, and delayed development. Beginning in childhood, affected individuals develop an insatiable appetite, which leads to chronic hyperphagia and obesity.

Answer 235

Prader-Willi syndrome

Question 236

HORMONAL CONTROL OF CALCIUM AND PHOSPHATE

Answer 236

HORMONAL CONTROL OF CALCIUM AND PHOSPHATE

Question 237

Both calcium and phosphate absorption in the GI tract are stimulated by the active form of __________.

Answer 237

vitamin D (calcitriol)

Question 238

where is 99% of total calcium?

Answer 238

bone

Question 239

How is the calcium stored as?

Answer 239

Mostly as complex calcium phosphate salts (hydroxyapatites).

Question 240

Bone remodeling involves the interplay between bone-building cells (_______) and cells that break down bone (________).

Answer 240

osteoblasts | osteoclasts

Question 241

Osteoblasts cause bone deposition and they secrete two proteins

Answer 241

RANK-L (Receptor Activator of Nuclear KappaB Ligand) | OPG (osteoprotegerin)

Question 242

function of RANK-L (Receptor Activator of Nuclear KappaB Ligand)?

Answer 242

This protein binds to the RANK receptor, which is expressed on precursor cells resulting in their differentiation into active osteoclasts. Active osteoclasts also express the RANK receptor, which, when stimulated, activates osteoclastic activity.

Question 243

function of OPG (osteoprotegerin)?

Answer 243

This protein binds RANK-L, there by preventing it from binding onto precursor or osteoclast cells. This reduces differentiation and overall osteoclastic activity. Thus, OPG acts as a “decoy” for RANK-L.

Question 244

which hormone influences bone remodeling?

Answer 244

parathyroid hormone (PTH)

Question 245

________ is well known for conserving bone integrity and it does so by at least two mechanisms. First, it induces the synthesis of OPG. Second, it reduces the secretion of cytokines by T-Lymphocytes. These cytokines stimulate differentiation of precursor cells into active osteoclasts and they stimulate activity of mature osteocytes. By inhibiting these cytokines and increasing OPG, this hormone reduces the activity of osteoclasts.

Answer 245

Estrogen

Question 246

Glucocorticoids function in bones

Answer 246

Glucocorticoids increase bone breakdown by inducing the synthesis and release of RANK-L and by inhibiting the synthesis of OPG.

Question 247

what Weight-bearing mechanical stress do to bones?

Answer 247

Weight-bearing mechanical stress increases the mineralization of bone.

Question 248

Actions of PTH in bone?

Answer 248

Increases Ca2+ reabsorption in distal tubule of the kidney Inhibits phosphate (Pi) reabsorption in proximal tubule of the kidney. Stimulates the 1-alpha-hydroxylase enzyme in kidney, converting inactive vitamin D to its active form. Causes bone resorption, releasing Ca2+ and Pi into the blood.

Question 249

role of Parathyroid Hormone-Related Peptide?

Answer 249

- PTHrP is a paracrine factor secreted by many tissues; e.g., lung, mammary tissue, placenta. - It may have a role in fetal development. In postnatal life, its role is unclear. - The majority of humoral hypercalcemias of malignancy are due to overexpression of PTHrP. - PTHrP has a strong structural homology to PTH and binds with equal affinity to the PTH receptor.

Question 250

Half of calcium in plasma is ______.

Answer 250

free calcium

Question 251

What displaces Ca2+ from protein?

Answer 251

Free H+

Question 252

What promotes resorption (BONE BREAKDOWN)?

Answer 252

RANK-L

Question 253

What reduces resorption?

Answer 253

OPG

Question 254

What regulates bone remodeling endogenously?

Answer 254

PTH endogenously promote RANK-L (bone resorption)

Question 255

What happens if you give a single OPG bolus and why?

Answer 255

reduce osteoclastic activity | DR. BRITT WILSON DOESNT KNOW

Question 256

Which t-lymphocytes activates osteoclasts?

Answer 256

IL-1, IL-6, TNF

Question 257

What do high glucocorticoids do?

Answer 257

Increase RANK-L | Decrease OPG

Question 258

What are things that breakdown weight bearing stress?

Answer 258

being sedentary bedridden weightlessness (astronauts)

Question 259

What happens in absence of weight bearing stress?

Answer 259

Plasma Ca2+ tends to be in the upper region or normal/ Plasma PTH decreases. Urinary calcium increases.

Question 260

Phosphate Trashy Hormone

Answer 260

PTH since it gets rid of phosphate

Question 261

another names for vitamin D3?

Answer 261

calcitriol | cholecalciferol

Question 262

What is the vitamin D3 synthesized in the skin and catalyzed by ultraviolet light?

Answer 262

7-Dehydrocholesterol

Question 263

What is the best indicator of total body stores of Vitamin D3?

Answer 263

25 OH Vitamin D (main circulating form but very low activity)

Question 264

Organs where PTH works?

Answer 264

Kidneys and bones

Question 265

Causes of hypercalcemia?

Answer 265

Lithium: Decrease responsiveness of PT gland to calcium Sarcoidosis & other granulomatous disorders: 1-alpha-OH -elevated thyroid hormone (osteoclasts?) -Milk-alkali syndrome (got milk and Tums?) Thiazide diuretics

Question 266

Drugs used to slow bone breakdown?

Answer 266

Bisphosphonates: calcitonin works quickly Etidronate Pamidroante Alendronate

Question 267

Function of Calcitonin

Answer 267

"Calcitonin Tones-down Calcium"

Question 268

clinical signs of hypoparathyroidism?

Answer 268

Trousseau's sign | Chvostek's Sign

Question 269

What can happen with a surgical removal of thyroid?

Answer 269

Hupomagnesemia; DiGeorge's syndrome since there no more PARAthyroid glands

Question 270

What can cause hypocalcemia?

Answer 270

``` alkalosis via hyperventilation transfusion of citrated blood rhabdomyolysis or tumor lysis subsequent hyperphosphatemia DiGeorge's syndrome ```

Question 271

Drugs used for osteoporosis | Denosumab

Answer 271

Blocks RANK-L

Question 272

Drugs used for osteoporosis | Teruparatide

Answer 272

Synthetic PTH

Question 273

Drugs used for osteoporosis | Calcitonin

Answer 273

"Calcitonin Tones-down Calcium"

Question 274

Drugs used for osteoporosis | Raloxifene

Answer 274

SERM

Question 275

Patient has: skull increase in size Skin overlying things, lower back, and skill warm to touch increased plasma ALP but normal CA2+ and Pi Increased urine hydrixyproline

Answer 275

Paget's disease: disorder of bone remodeling

Question 276

Treatment for Paget's disease?

Answer 276

Bisphosphonates: Etidronate Pamidroante Alendronate

Question 277

To sense the free calcium, the parathyroid cell depends upon high levels of expression of the ______.

Answer 277

calcium-sensing receptor (CaSR)

Question 278

Calcitonin (CT) is a peptide hormone secreted by the __________ of the thyroid gland. It is released in response to elevated free calcium.

Answer 278

parafollicular cells (C cells)

Question 279

function of calcitonin?

Answer 279

- Calcitonin lowers plasma calcium by decreasing the activity of osteoclasts, thus decreasing bone resorption. Calcitonin is useful in the treatment of Paget’s disease, severe hypercalcemia, and osteoporosis. - Calcitonin is not a major controller of Ca2+ in humans. Removing the thyroid (with the C cells) or excess of calcitonin via a C cell tumor (med- ullary carcinoma of the thyroid) has little impact on plasma calcium. - No deficiency or excess disease has been described.

Question 280

Differences in vitamin D2 and D3?

Answer 280

Vitamin D2 (ergocalciferol) is a vitamin but can functionally be considered a prohormone. It is a normal dietary component. A slightly different form, vitamin D3 (cholecalciferol), is synthesized in the skin. Its active form (1,25 di-OH D3) is a hormone secreted by cells of the kidney’s proximal tubule.

Question 281

How many days do biphosphonates need to be fully active?

Answer 281

Bisphosphonates need 2-3 days to be fully effective

Question 282

What is Chvostek’s sign?

Answer 282

Chvostek’s sign is induced by tapping the facial nerve just anterior to the ear lobe.

Question 283

What is Trousseau’s sign?

Answer 283

Trousseau’s sign is elicited by inflating a pressure cuff on the upper arm. A positive response is carpal spasm.

Question 284

- This is a rare familial disorder characterized by target tissue resistance to parathyroid hormone. - Exhibits same signs and symptoms as primary hypoparathyroidism except PTH elevated - It is usually accompanied by developmental defects: mental retardation, short and stocky stature, one or more metacarpal or metatarsal bones missing (short 4th or 5th finger).

Answer 284

Pseudohypoparathyroidism

Question 285

Predictive indices for a secondary disorder: When the plasma calcium and phosphate are changing in the same direction, the origin is usually a secondary disorder. - Secondary hyperparathyroidism: ___________ - Secondary hypoparathyroidism: ____________

Answer 285

both decrease both increase

Question 286

What is this: - It is a loss of bone mass (both mineralization and matrix) with fractures, due to normal age-related changes in bone remodeling as well as additional factors that exaggerate this process. - Bone mass reaches a peak subsequent to puberty. Heredity accounts for most of the variation but physical activity, nutrition, and reproductive hormones play a significant role, especially estrogens even in men. - Secondary ________ can occur in thyrotoxicosis and particularly with elevations in glucocorticoids. - A mainstay of treatment involves the use of bisphosphonates that are rapidly incorporated into bone and reduce the activity of osteoclasts. - Calcitonin inhibits bone resorption

Answer 286

Osteoporosis

Question 287

Diagnosing lab results: - If bone mineral density is 2.5 standard deviations below the average, then this equals to _____. - If bone mineral density is 1 to 2.5 standard deviations below the average, then this equals _____.

Answer 287

Osteoporosis osteopenia

Question 288

Osteoporosis treatment:

Answer 288

Osteoporosis can also be treated with: - Denosumab: inhibitor of RANKL. RANKL is a TNF family of cytokine that activates osteoclasts; denosumab therefore, inhibits osteoclasts. - Teriparatide: synthetic PTH. When used intermittently, teriparatide has a stimulatory effect on osteoblastic bone formation. - Calcitonin - Raloxifene: selective estrogen receptor modifier

Question 289

What is this: -Origin is the abnormal mineralization of bone and cartilage. -before plate closure -expansion of the epiphyseal plates and the most striking abnormalities are the bowing of the legs and protuberant abdomen -Most common cause in adults is a malabsorption disorder, e.g., celiac disease; a vitamin D deficiency can also cause -Rarely caused by enzyme deficiencies when substrate availability is normal.

Answer 289

Rickets

Question 290

What is this: -Origin is the abnormal mineralization of bone and cartilage. -after plate closure -symptoms are more subtle. -Most common cause in adults is a malabsorption disorder, e.g., celiac disease; a vitamin D deficiency can also cause -Rarely caused by enzyme deficiencies when substrate availability is normal.

Answer 290

osteomalacia

Question 291

Difference between rickets and osteomalacia?

Answer 291

Rickets is before plate closure, osteomalacia is after plate closure.

Question 292

Function of PTH at kidneys?

Answer 292

At the kidney, PTH: (1) increases distal tubule calcium reabsorption (2) inhibits proximal tubule phosphate reabsorption (3) stimulates the 1-alphahydroxylase enzyme.

Question 293

The most common cause of hypercalcemia is:

Answer 293

primary hyperparathyroidism (↑ calcium, ↓ phosphate).

Question 294

The most common cause of primary hypoparathyroidism is:

Answer 294

surgery (↓ calcium, ↑ phosphate).

Question 295

Vitamin D de ciency induces a secondary hyperparathyroidism (___ calcium, ___ phosphate) and a decrease in bone mass (rickets, osteomalacia).

Answer 295

(↓ calcium, ↓ phosphate)

Question 296

Vitamin D excess induces a ________ and the increased activity of vitamin D directly decreases bone mass.

Answer 296

secondary hypoparathyroidism (↑ calcium, ↑ phosphate)

Question 297

Chronic renal failure often induces a hyperphosphatemia and a _________.

Answer 297

secondary hyperparathyroidism (↓ calcium, ↑ phosphate).

Question 298

THYROID HORMONES

Answer 298

THYROID HORMONES

Question 299

How much iodine or iodide do we need to take every day?

Answer 299

Dietary intake of about 500 μg per day is typical, mainly in the form of iodide (I–) or iodine (I). To maintain normal thyroid hormone secretion, 150 μg is the minimal intake necessary. I– is the form absorbed from the small intestine.

Question 300

The functional unit of the thyroid gland is the _____.

Answer 300

follicle

Question 301

The lumen is filled with thyroglobulin, which contain large numbers of ______.

Answer 301

thyroid hormone molecules

Question 302

Surrounding the lumen are the follicle cells, which function to:

Answer 302

both synthesize and release thyroid hormones.

Question 303

Iodine uptake is via a sodium/potassium pump powered sodium/iodide symporter on the basal membrane (NIS). is pump can raise the concentration of I ̄ within the cell to as much as 250 times that of plasma. The pump can be blocked by anions like perchlorate and thiocyanate, which compete with I. Along the apical membrane, the I ̄ is transported into the lumen by an anion- exchanger called _____.

Answer 303

pendrin

Question 304

Enough hormone is stored as iodinated thyroglobulin in the follicular colloid to last the body for ______.

Answer 304

2–3 months

Question 305

T3 and T4 Half life:

Answer 305

T4 half-life = 6 days | T3 half-life = 1 day

Question 306

Thyroid hormone and cholesterol:

Answer 306

Thyroid hormone accelerates cholesterol clearance from the plasma.

Question 307

Thyroid hormone and the Eyes?

Answer 307

Thyroid hormones are required for conversion of carotene to vitamin A, and, as a consequence, hypothyroid individuals can suffer from night blindness and yellowing of the skin.

Question 308

Where does the thyroid hormone act on the heart?

Answer 308

- Acting on the SA node, they directly increase heart rate. - Cardiac output is increased, and both heart rate and stroke volume are elevated. - Systolic pressure increases are due to increased stroke volume, and diastolic pressure decreases are due to decreased peripheral resistance. - Thyroid hormones in the normal range are required for optimum cardiac performance.

Question 309

main cause of Primary Hypothyroidism?

Answer 309

Most common cause is Hashimoto’s thyroiditis, an autoimmune destruction of the thyroid with lymphocytic infiltration; ↑ TPO antibodies; early stages have a diffusely enlarged thyroid progressing in the later stages to a smaller atrophic and fibrotic gland.

Question 310

end stage of untreated hypothyroidism?

Answer 310

Myxedema coma is the end stage of untreated hypothyroidism. The major features are hypoventilation, fluid and electrolyte imbalances, and hypothermia and ultimately shock and death.

Question 311

results of Untreated postnatal hypothyroidism?

Answer 311

Untreated postnatal hypothyroidism results in cretinism, a form of dwarfism with mental retardation.

Question 312

What is this: - untreated hypothyroidism - Individuals often appear normal following delivery but may display some respiratory difficulty, jaundice, feeding problems, and hypotonia. - Abnormalities rapidly develop in nervous system maturation, which are irreversible and result in mental retardation. - Prepubertal growth, including bone ossification, is retarded in the absence of thyroid hormones. - stippled epiphysis - There is no evidence that thyroid hormones act directly on growth or bone formation. Rather, thyroid hormone appears to be permissive or act synergistically with growth hormone or growth factors acting directly on bone. - Acquired hypothyroidism during childhood results in dwarfism but there is no mental retardation. - At puberty, increased androgen secretion drives an increased growth hormone secretion. This will not occur with depressed levels of thyroid hormones.

Answer 312

Cretinism

Question 313

another name for Primary Hyperthyroidism

Answer 313

Graves’ Disease

Question 314

_________ by definition is the clinical syndrome whereby tissues are exposed to high levels of thyroid hormone (= hyperthyroidism)

Answer 314

Thyrotoxicosis

Question 315

The most common cause of thyrotoxicosis is ____________, a primary hyperthyroidism.

Answer 315

Graves’ disease

Question 316

What is Graves’ disease?

Answer 316

Graves’ disease is an autoimmune problem in which one antibody is directed against the thyroid receptor. It is referred to as the thyroid stimu- lating antibody (TSI or TSH-R). In addition TPO antibodies and those against thyroglobulin are also found in Graves’ disease.

Question 317

What do you look for in a patient with Grave's disease by just looking at them?

Answer 317

The wide-eyed stare (exophthalmos) in patients with Graves’ is caused by an infiltration of orbital soft tissues and extraocular muscles and the resulting edema, and this process is caused by the antibodies.

Question 318

Untreated hyperthyroidism may decompensate into a condition called

Answer 318

Untreated hyperthyroidism may decompensate into a condition called “thyroid storm.”

Question 319

Acute treatment of Grave's disease

Answer 319

l Beta blockers are the most rapid in effect l Methimazole or propylthiouracil stops the production of hormone l Iodine in high dose stops incorporation of iodine into the gland l Steroids such as dexamethasone stop conversion of T4 to T3 l Long-term permanent cure is ablation of the gland with radioactive iodine

Question 320

What is goiter?

Answer 320

A goiter is simply an enlarged thyroid and does not designate functional status. A goiter can be present in hypo-, hyper-, and euthyroid states. There is no correlation between thyroid size and function.

Question 321

What catalizyes oxidation, iodination and coupling?

Answer 321

Peroxidase

Question 322

What blocks oxidation, iodination and coupling?

Answer 322

Thiomides (propulthiouiracil and methimazole)

Question 323

Why are T4 made more than T3?

Answer 323

More DIT than MIT

Question 324

Whats the Wolff-Chaikoff effect?

Answer 324

the increase in iodine causes temporary decrease in thyroid hormone secretion

Question 325

Thyroxine (T4) + activation via 5' monodeiodianse =

Answer 325

T3

Question 326

Thyroxine (T4) + degradation via 5' monodeiodianse =

Answer 326

Reverse T3

Question 327

Low done makes _____ T3 and _____ T4

Answer 327

more T3 and Less T4

Question 328

GROWTH HORMONE

Answer 328

GROWTH HORMONE

Question 329

name all anabolic hormones

Answer 329

anabolic hormones (i.e., growth hormone, insulin, thyroid hormones, and androgens)

Question 330

First noted sign in puberty in females and males and why?

Answer 330

First noted sign in a female is breast development; first by estrogen (promotes duct growth) then progesterone (promotes development of milk-producing alveolar cells). First noted sign in a male is enlargement of the testes (mainly FSH stimulating seminiferous tubules).

Question 331

Pubic hair development in males and females is dependent on _________.

Answer 331

androgen

Question 332

When does growth spur occur in females and in males?

Answer 332

In females, the growth spurt begins early in puberty and is near completion by menarche. In males, the growth spurt develops near the end of puberty.

Question 333

What is this: - It is caused by a post pubertal excessive secretion of growth hormone. - It is almost always due to macroadenoma (> 1 cm dia) of the anterior pituitary and second in frequency to prolactinomas. - There is a slow onset of symptoms, and the disease is usually present for 5 to 10 years before diagnosis. - There is characteristic proliferation of cartilage, bone and soft tissue, visceral, and cardiomegaly. - Observable changes include enlargement of the hands and feet (acral parts) and coarsening of the facial features, including downward and forward growth of the mandible. Also, increased hat size. - Measurement of IGF-I is a useful screening measure and confirms diagnosis with the lack of growth hormone suppression by oral glucose.

Answer 333

acromegaly

Question 334

How do you diagnose acromegaly?

Answer 334

- Elevated IGF level - Failure of suppression of GH/IGF after giving glucose - MRI shows lesion in brain in pituitary

Question 335

Treatment for acromegaly?

Answer 335

Surgical removal by trans-sphenoidal approach is first. Removal of an over-producing adenoma is the first treatment in most of endocrinology with the exception of prolactinoma.

Question 336

What is used for treatment if surgery fails?

Answer 336

If surgical removal fails, use the growth hormone receptor antagonist, pegvisomant, or octreotide. Octreotide is synthetic somatostatin. Cabergoline is a dopamine agonist used when other medications have failed.

Question 337

if surgery and other methods fail, what is the last resort treatment?

Answer 337

Radiation is used last, only after surgery, pegvisomant, octreotide and cabergoline have failed.

Question 338

Where is GnRH made and what does it release?

Answer 338

GnRH—synthesized in preoptic region of hypothalamus and secreted in pulses into hypophyseal portal vessels • produces pulsatile release of LH and FSH • pulsatile release of GnRH prevents downregulation of its receptors in anterior pituitary

Question 339

Where is LH and FSH made and what does it secrete?

Answer 339

LH and FSH—produced and secreted by gonadotrophs of anterior pituitary • LH stimulates Leydig cells to produce testosterone. • FSH stimulates Sertoli cells

Question 340

What produces produces negative feedback for LH?

Answer 340

Leydig cell testosterone—some diffuses directly to Sertoli cells, where it is required for Sertoli cell function. • produces negative feedback for LH

Question 341

What produces negative feedback for FSH?

Answer 341

Sertoli cell inhibin B—produces negative feedback for FSH

Question 342

What is the substance responsible for this? - Some target tissue express this enzyme, which converts testosterone into the more potent dihydrotestosterone. - Sexual differentiation: differentiation to form male external genitalia l Growth of the prostate - Male-pattern baldness - Increased activity of sebaceous glands - Synthesis of NO synthase in penile tissue

Answer 342

5a-reductase

Question 343

What provides the nourishment that is required for normal spermatogenesis?

Answer 343

Sertoli cells

Question 344

DEFINE: any steroid that controls the development and maintenance of masculine characteristics

Answer 344

Androgen

Question 345

DEFINE: a natural male androgen of testicular origin, controlled by the luteinizing hormone (LH)

Answer 345

Testosterone

Question 346

DEFINE: a more active form of testosterone made by 5-alpha-reductase. It makes the penis, prostate, and scrotum on an embryo.

Answer 346

Dihydrotestosterone

Question 347

DEFINE: a synthetic androgen, which is an anabolic steroid sometimes used by athletes

Answer 347

Methyl testosterone

Question 348

DEFINE: natural weak androgens (male and female) of adrenal origin, controlled by ACTH. These are DHEA and androstenedione.

Answer 348

Adrenal androgens

Question 349

DEFINE: peptide hormones secreted into the blood. They inhibit the secretion of FSH by pituitary gonadotrophs.

Answer 349

Inhibins

Question 350

# DEFINE: an enzyme that stimulates the aromatization of the A-ring of testosterone, converting it into estradiol. e physiologic importance of this conversion is not understood; however, approximately a third of the estradiol in the blood of men arises from Sertoli cells, and the remainder arises from peripheral conversion of tes- tosterone to estradiol by an aromatase present in adipose tissue. One sign of a Sertoli cell tumor is excessive estradiol in the blood of the a ected man.

Answer 350

Aromatase

Question 351

Normal male development requires the presence of 3 hormones:

Answer 351

testosterone, dihydrotestosterone, and the Müllerian inhibiting factor (MIF).

Question 352

Why are men built bigger than women?

Answer 352

The capacity of androgens to stimulate protein synthesis and decrease protein breakdown, especially in muscle, is responsible for the larger muscle mass in men as compared with women. Exogenous androgens (anabolic steroids) are sometimes taken by men and women in an attempt to increase muscle mass.

Question 353

Normally, the scrotum provides an environment that is _______ °C cooler than the abdominal cavity. e cooling is accomplished by a countercurrent heat exchanger located in the spermatic cord. Also, the temperature of the scrotum and the tes- tes is regulated by relative degree of contraction or relaxation of the cremasteric muscles and scrotal skin rugae that surround and suspend the testes.

Answer 353

4 °C cooler

Question 354

Erection: Symphathetic or parasympathetic?

Answer 354

(a parasympathetic response) Erection is caused by dilation of the blood vessels in the erectile tissue of the penis (the corpora- and ischiocav- ernous sinuses).

Question 355

This dilation increases the inflow of blood so much that the penile veins get compressed between the engorged cavernous spaces and the Buck’s and dartos fasciae. _______, working through cGMP, mediates the vasodilation.

Answer 355

Nitric oxide (NO)

Question 356

What is Emission?

Answer 356

Emission is the movement of semen from the epididymis, vas deferens, seminal vesicles, and prostate to the ejaculatory ducts.

Question 357

Emission: Symphathetic or parasympathetic?

Answer 357

The movement is mediated by sympathetic (thoracolumbar) adrenergic transmitters.

Question 358

how is ejaculation caused?

Answer 358

- Ejaculation is caused by the rhythmic contraction of the bulbospongiosus and the ischiocavernous muscles, which surround the base of the penis. - Contraction of these striated muscles that are innervated by somatic motor nerves causes the semen to exit rapidly in the direction of least resistance, i.e., outwardly through the urethra.

Question 359

Causes of Hypogonadism:

Answer 359

- Noonan syndrome - Klinefelter’s syndrome - Hypothalamic-pituitary disorders (Kallman’s syndrome, panhypopituitarism) - Gonadal failure/sex steroid synthesis failure

Question 360

DEFINE: an individual with the genetic constitution and gonads of one sex and the genitalia of the other.

Answer 360

Pseudohermaphrodite

Question 361

DEFINE: female fetus exposed to androgens during the 8th to 13th week of development, e.g., congenital virilizing adrenal hyperplasia.

Answer 361

Female pseudohermaphroditism

Question 362

DEFINE: lack of androgen activity in male fetus, e.g., defective testes, androgen resistance

Answer 362

Male pseudohermaphroditism

Question 363

Eyaculation: Symphathetic or parasympathetic?

Answer 363

ejaculation requires sympathetic involvement.

Question 364

Days in the menstrual cycle?

Answer 364

menstrual cycle (approximately 28 days)

Question 365

What is the first day of bleeding of the menstrual cycle called?

Answer 365

By convention, the first day of bleeding (menses) is called day 1 of the menstrual cycle.

Question 366

Name the Phases of the menstrual cycle.

Answer 366

1. Follicular phase 2. Ovulation phase 3. Luteal phase 4. Menses

Question 367

Phase of the menstrual cycle that (first 2 weeks) is also called the proliferative or preovulatory phase. This phase is dominated by the peripheral effects of estrogen, which include the replacement of the endometrial cells lost during menses.

Answer 367

Follicular phase

Question 368

Phase of the menstrual cycle that (approximately day 14) is preceded by the LH surge, which induces ovulation.

Answer 368

Ovulation phase

Question 369

Phase of the menstrual cycle that (approximately 2 weeks) is dominated by the elevated plasma levels of progesterone, and along with lower levels of secreted estrogen, creates a secretory quiescent endometrium that prepares the uterus for implantation.

Answer 369

Luteal phase

Question 370

Phase of the menstrual cycle that Withdrawal of the hormonal support of the endometrium at this time causes necrosis and menstruation.

Answer 370

Menses

Question 371

Menstrual cycle phase 1 - 14 is called

Answer 371

follicular phase

Question 372

DEFINE: atretic

Answer 372

to die

Question 373

________ promotes growth and increased sensitivity to FSH; thus the follicle continues to develop. The remaining follicles, lacking sufficient FSH, synthesize only androgen and become atretic (die).

Answer 373

Estradiol

Question 374

What Possess the follicle’s only FSH and what is its function?

Answer 374

Granulosa Cells: Possess the follicle’s only FSH receptors. When coupled to FSH, these act via cAMP to increase the activity of aromatase; aromatase converts the androgens to estrogens (mainly estradiol).

Question 375

How do you calculate ovulation day?

Answer 375

Cycle length – 14 = ovulation day

Question 376

Menstruation is due to a lack of _______

Answer 376

a lack of gonadal sex steroids.

Question 377

What is the main circulating estrogen following menopause?

Answer 377

Estrone: Some is secreted from the ovary but much is formed in peripheral tissues such as adipose tissue from androgens. These androgens originate from both the ovary and the adrenal glands. This is the main circulating estrogen following menopause. Fat cells have aromatase. Adipose tissue creates modest levels of estrogen.

Question 378

Define: Amenorrhea

Answer 378

amenorrhea means the lack of menstral bleeding.

Question 379

What causes amenorrhea?

Answer 379

- In the absence of anatomic abnormalities (and pregnancy), it usually indicates a disruption of the hypothalamic–pituitary axis or an ovarian problem. - A hypothalamic–pituitary origin would include Kallman’s syndrome, functional hypothalamic amenorrhea, amenorrhea in female athletes, eating disorders, hypothyroidism (possibly because high TRH stimulates prolactin), and pituitary tumors such as prolactinomas. - Ovarian causes could be premature ovarian failure (premature meno- pause), repetitive ovulation failure, or anovulation (intermittent bleeding), or a polycystic ovary.

Question 380

What is this: - Characterized by elevated LH/FSH ratio. - Clinical signs include: infertility, hirsutism, obesity, insulin resistance, and amenorrhea or oligomenorrhea - The enlarged polycystic ovaries are known to be associated with increased androgen levels (DHEA). - It originates in obese girls. The high extraglandular estrogens (mainly estrone) selectively suppress FSH. Ovarian follicles do have a suppressed aromatase activity and thus a diminished capacity to convert androgen into estrogen, but the adrenals may also contribute to the excess androgens as well. - High androgens promote atresia in developing follicles and disrupt feedback relationships. Look for high LH and DHEA levels. - The overall result is anovulation-induced amenorrhea with an estrogen- induced endometrial hyperplasia and breakthrough bleeding. - Although poorly understood the hyperinsulinemia is believed to be a key etiologic factor.

Answer 380

Polycystic Ovarian Syndrome

Question 381

Treatment for amenorrhea in PCOS

Answer 381

metformin

Question 382

Treat androgenization with:

Answer 382

spironolactone

Question 383

What is this: - Defined as an excessive generally male pattern of hair growth. - Virilization refers to accompanying additional alterations, such as deepening of the voice, clitoromegaly, increased muscle bulk, and breast atrophy. - It is often associated with conditions of androgen excess such as congenital adrenal hyperplasia and polycystic ovarian syndrome. - Axillary and pubic hair are sensitive to low levels of androgen. - Hair on the upper chest, face (scalp region not involved), and back requires more androgen and represents the pattern seen in males. - Circulating androgens involved are testosterone, DHEA, DHEAS, and androstenedione in response to LH and ACTH. - Measurements of DHEAS as well as a dexamethasone suppression test helps in separating an adrenal from an ovarian source. - Polycystic ovarian syndrome is the most common cause of ovarian androgen excess.

Answer 383

Hirsutism

Question 384

what constitutes Low sperm count?

Answer 384

Low sperm counts (<20 million/mL of ejaculate)

Question 385

Within a week or two of fertilization, trophoblastic cells of the placenta begin secreting hCG. What is the function go hCG?

Answer 385

In short, hCG prevents regression of the corpus luteum, thus allowing it to continue producing estrogens and proges- terone.

Question 386

Why do we check hCG?

Answer 386

hCG doubles in the early weeks of pregnancy. Because it maintains secretion of progesterone from the corpus luteum, progesterone is a sensitive marker of early fetal well-being.

Question 387

What are some markers for fetal well-being?

Answer 387

hPL (hCS) is secreted in proportion to the size of the placenta and is an index of placental well-being. hCG doubles in the early weeks of pregnancy. Because it maintains secretion of progesterone from the corpus luteum, progesterone is a sensitive marker of early fetal well-being. Estriol: The placenta expresses aromatase. This enzyme converts the A and tes- tosterone from the fetus into estrogens, estriol being the primary one. Thus, estriol becomes a good marker for fetal well-being.

Question 388

Why is there no hypertension in a pregnancy?

Answer 388

Cardiac output increases but peripheral resistance decreases and as a result there is no hypertension associated with a normal pregnancy (parallel circuit of placenta)

Question 389

obstetric hemorrhage =

Answer 389

Sheehan syndrome

Question 390

The pubic symphysis, cervix, and vagina become more distensible. ese changes make passage of the fetus through the birth canal easier. The peptide hormone __________, which is secreted by the placenta, also promotes these changes. Its action is not essential.

Answer 390

relaxin

Question 391

_______ cause contraction of the uterus and are thought to initiate the labor process.

Answer 391

Prostaglandins When a fetus dies, toxic products originating from the fetus increase prostaglandin release in the uterus, thus initiating contractions and a spontaneous abortion (miscarriage). Similarly, administration of prostaglandins induces abortion.

Question 392

Breast feeding is a form of contraceptive???

Answer 392

Yes, For the suckling stimulus to inhibit GnRH secretion completely, the stimulus must be prolonged and frequent. Supplementation of the mother’s milk with other fluids or sources of energy reduces the baby’s suckling and allows gonadotropin secretion, follicular growth, and ovulation to occur. Breastfeeding is a form of contraceptive because it should stop ovulation.

Question 393

GASTROINTESTINAL

Answer 393

GASTROINTESTINAL

Question 394

What are the layers of the gastrointestinal tract?

Answer 394

Mucosa Submucosa Muscularis externa Serosa

Question 395

What does norepinephrine (NE) do in the gastrointestinal (GI) system?

Answer 395

↓ motility ↓ secretions ↑ constriction of sphincters An increase in sympathetic activity slows processes.

Question 396

What does ACh do in the gastrointestinal (GI) system?

Answer 396

↑ motility | ↑ secretions

Question 397

What does VIP do in the gastrointestinal (GI) system?

Answer 397

↓ constriction of sphincters

Question 398

What does GRP do in the gastrointestinal (GI) system?

Answer 398

↑ gastrin

Question 399

What is VIP?

Answer 399

VIP = vasoactive intestinal peptide, an inhibitory parasympathetic transmitter

Question 400

What is GRP?

Answer 400

GRP = gastrin-releasing peptide; stimulates the release of gastrin from G cells

Question 401

Oscillation of membrane potential is generated by interstitial cells (inter-stitial cells of ________) that act as pacemakers. This is referred to as slow waves or basic electrical rhythm, and if threshold is reached it generates action potentials.

Answer 401

Cajal

Question 402

What is this: - Failure of the LES to relax, resulting in swallowed food being retained in the esophagus - Caused by abnormalities in the enteric nerves - Peristaltic waves are weak

Answer 402

Achalasia

Question 403

What is this: - LES doesn’t maintain tone - Acid reflux damages esophageal epithelium

Answer 403

Gastroesophageal reflux disease (GERD)

Question 404

What is this: - Spasms of esophageal muscle - Presents with characteristics of a heart attack (e.g., chest pain) - Barium swallow shows repeated, spontaneous waves of contraction

Answer 404

Diffuse esophageal spasm

Question 405

What is Dysphagia?

Answer 405

difficulty in swallowing.

Question 406

Migrating Motor Complex (MMC)

Answer 406

- A propulsive movement initiated during fasting that begins in the stomach and moves undigested material from the stomach and small intestine into the colon. - Repeats every 90–120 minutes during fasting. - When one movement reaches the distal ileum, a new one starts in the stomach. - Correlated with high circulating levels of motilin, a hormone of the small intestine - This movement prevents the backflow of bacteria from the colon into the ileum and its subsequent overgrowth in the distal ileum.

Question 407

What do Parietal cells secrete?

Answer 407

HCl Intrinsic factor combines with vitamin B12 and is reabsorbed in the distal ileum. This is the only substance secreted by the stomach that is required for survival. It is released by the same stimuli that release HCl.

Question 408

What do Chief Cells secrete?

Answer 408

Pepsinogen

Question 409

What do Mucous Neck Cells secrete?

Answer 409

protective mucus, HCO3 combination

Question 410

There are 3 natural substances that stimulate parietal cells:

Answer 410

- Acetylcholine (ACh), acting as a transmitter; release is stimulated by sight/smell of food and reflexly in response to stomach distension (vagovagal reflex). - Locally released histamine; stimulated by Ach and gastrin - The hormone gastrin; stimulated by release of GRP

Question 411

As stomach pH falls, ________ is released, which inhibits gastrin and reduces acid secretion (feedback regulation of acid secretion).

Answer 411

somatostatin (SST)

Question 412

Most of the control of pancreatic secretion is via:

Answer 412

secretin and CCK

Question 413

What makes poop yellow?

Answer 413

A major bile pigment, bilirubin is a lipid-soluble metabolite of hemoglobin. Transported to the liver attached to protein, it is then conjugated and excreted as water-soluble glucuronides. ese give a golden yellow color to bile.

Question 414

What makes poop brown?

Answer 414

Stercobilin is produced from metabolism of bilirubin by intestinal bacteria. It gives a brown color to the stool.

Question 415

Increased levels of plasma bilirubin produce _______. If severe, bilirubin can accumulate in the brain, producing profound neurological disturbances (_________).

Answer 415

jaundice kernicterus

Question 416

What is celiac disease?

Answer 416

``` Celiac disease is an immune reaction to gluten (protein found in wheat) that damages intestinal cells; the end result is diminished absorptive capacity of the small intestine. ```

Question 417

Hartnup’s disease

Answer 417

Many of the amino acid transporters are selective for speci c amino acids. Hartnup’s disease is a genetic deficiency in the transporter for tryptophan.

Question 418

REGION OF THE GASTRO INTESTINAL TRACT? - Hypertonic fluid enters this region, and following the movement of some water into the lumen, the fluid becomes and remains isotonic. - The absorption of most divalent ions and water-soluble vitamins begins here and continues through the small intestine. - Injested iron and calcium tend to form insoluble salts. The acid environment of the stomach redissolves these salts, which facilitates their absorption in the small intestine. Iron and calcium absorption is diminished in individuals with a deficient stomach acid secretion. - Calcium absorption is enhanced by the presence of calbindin in intestinal cells, and calcitriol (active vitamin D) induces the synthesis of this protein. - Intestinal cells express the protein ferritin, which facilitates iron absorption.

Answer 418

Duodenum

Question 419

REGION OF THE GASTRO INTESTINAL TRACT? - Overall, there is a net reabsorption of water and electrolytes. - The cellular processes involved are almost identical to those described in the renal physiology section for the cells lining the nephron proximal tubule.

Answer 419

Jejunum

Question 420

REGION OF THE GASTRO INTESTINAL TRACT? - Net reabsorption of water, sodium, chloride, and potassium continues, but there begins a net secretion of bicarbonate. - It is in the distal ileum, and only in the distal ileum, where the reabsorp- tion of bile salts and intrinsic factor with vitamin B12 takes place.

Answer 420

Ileum

Question 421

REGION OF THE GASTRO INTESTINAL TRACT? - This part does not have digestive enzymes or the protein transporters to absorb the products of carbohydrate and protein digestion. - Also, because bile salts are reabsorbed in the distal ileum, very few lipid- soluble substances are absorbed in the colon. - There is a net reabsorption of water and sodium chloride, but there are limitations. - Most of the water and electrolytes must be reabsorbed in the small intestine, or the it becomes overwhelmed. - Most of the water and electrolytes are absorbed in the ascending and transverse colon; thereafter, it has mainly a storage function. - The colon is a target for aldosterone, where it increases sodium and water reabsorption and potassium secretion. - Because there is a net secretion of bicarbonate and potassium, diarrhea usually produces a metabolic acidosis and hypokalemia. It commonly presents as hyperchloremic, nonanion gap metabolic acidosis, as described in the acid-base section.

Answer 421

Colon

Question 422

what is diarrhea?

Answer 422

Except for the infant where it can be hypotonic, diarrhea is a loss of isotonic fluid that is high in bicarbonate and potassium.